Isolated oculomotor disorders caused by central nervous system damage are quite rare. As a rule, they are combined with other signs of cerebral trunk damage. A clinical case with the focus of amyelination in the cerebral trunk area, which manifests itself in the form of bilateral horizontal gaze palsy in the absence of other focal neurological symptoms is presented. A complete regression of oculomotor disorders was observed against the background of glucocorticosteroid therapy. A differential research was carried out among amyelinating, ophthalmic, endocrinologic diseases, ANCA-associated vasculitis (AAV).

A medical case of an acute demyelinating process in cerebrum caused by taking levamisole is presented. The issues of pathogenesis and differential diagnosis of levamisole-induced leukoencephalopathy with acute disseminated encephalomyelitis, multiple sclerosis, progressive multifocal leukoencephalopathy, and cerebral lymphoma are discussed.

Multiple sclerosis is a chronic demyelinating and neurodegenerative disease of the central nervous system, in which autoimmune inflammation and oxidative stress play essential pathogenetic roles. Activation and infiltration of immune cells in brain tissues, lipid peroxidation products, mitochondrial dysfunction, defective antioxidant protection, and many other pathological factors result in demyelination, axonal injury and death, and apoptosis of oligodendrocytes and neurons, all of which causes constant progression of the disease. The new oral agent for the treatment of relapsing-remitting multiple sclerosis (RRMS), dimethyl fumarate (DMF), helps change the pathogenetic mechanisms of the disease, thus decreasing the rate of exacerbations, slowing down disease progression, and reducing the risk of radiological progression of the disease.

Dimethyl fumarate (DMF) is a new oral option for disease-modifying therapy (DMT) in patients with remitting multiple sclerosis as a first line treatment. The results of international randomized studies comparing DMF with placebo and other DMTs are presented. DMF is a DMT with promised efficacy and favorable safety profile that could be a treatment option for patients with suboptimal response for other first line DMTs and used as initial therapy for treatment-naive patients with unfavorable prognostic factors.

Multiple sclerosis (MS) is the most common and potentially disabling disease of the central nervous system in young people. Not only inflammatory, but also neurodegenerative processes are involved in the pathogenesis of MS. The use of MS-modifying drugs (MSMDs) has led to a substantial reduction in the frequency of MS exacerbations and to the slower development of irreversible neurological deficit. Glatiramer acetate is one of the MSMDs of first choice and has a dual (anti-inflammatory and neuroprotective) action. The drug has proven to be effective and safe if administered long-term. Therapy with glatiramer acetate has been established to promote the production of anti-inflammatory cytokines and neurotrophic factors, which prevent the development of a degenerative process and stimulate remyelination, and to slow the progression of cerebral atrophy. Experimental findings suggest that the drug improves the processes of neurogenesis.The efficiency of treatment is known to be associated with patient medication adherence. This largely depends on the frequency and route of drug administration and on the development of adverse events (AEs). To improve treatment adherence to glatiramer acetate, its new 40-mg formulation has been designed, which allows it to be administered only thrice weekly. The use of the formulation has demonstrated its efficacy and safety and resulted in a considerable reduction in the incidence rate of AEs.

AIM:To specify the pathogenetic link between blood supply of the bladder neck and lower urinary tract symptoms (LUTS).MATERIAL AND METHODS:The study involved 78 men aged 26 to 50 years, including 19 patients with multiple sclerosis (MS) and LUTS, 29 patients with chronic prostatitis category IIIB with LUTS and 30 patients with chronic prostatitis category IIIB without LUTS (control group). All the patients underwent Doppler ultrasonography of prostatic arteries and selective study of blood flow in the neck of the bladder. Pharmacological test using combinations of 1-blockers (1-AB) with m-anticholinergics (m-CB) and phosphodiesterase type 5 inhibitors (PDEI-5).RESULTS:The changes in the blood circulation of VUS were found to correlate with LUTS. The response of blood flow depended not only on the type of pharmacological agents, but also on the degree of vascular changes and neurological deficit in VUS.DISCUSSION:The findings of VUS vascular pharmacological tests with PDEI-5 and 1-AB + m-CB were comparable in chronic prostatitis with non-neurogenic LUTS and in MS with neurogenic LUTS. Vascular reaction in VUS depends on the presence of neurological deficit. The combination of (1-AB+ m-CB) increases the blood circulation of the bladder neck and prostate and reduces the LUTS. PDEI-5 reduces LUTS due to the positive effect on the blood circulation of the prostate and VUS.CONCLUSION:Circulatory abnormalities (=hypoxia) in VUS is an important pathogenetic mechanism of neurogenic and non-neurogenic LUTS and the way to compensate them using a combination of (1-AB+ m-CB) or PDEI-5. Therefore, one of the mechanisms of LUTS is associated with impaired blood flow in the bladder neck and VUS.

The article presents the results of researches concerning preventive therapy, relapse treatment and symptomatic treatment of multiple sclerosis, neuromyelitis optica and neuromyelitis optica spectrum disorders. The medicines of first and second line that modulate multiple sclerosis course (modifying medicines) are reviewed. The data about new testing drugs are presented.

The article presents the result of a study of efficacy and safety of the medicine from the group of monoclonal antibodies – natalizumab (tisabri) in remitting-relapsing multiple sclerosis. The medicine significantly decreases the relapse rate and disease progression. This data confirmed by MRI. The opportunity of prescribing natalizuab as a first line drug is discussed. The indications and contraindications to its use are presented. We pay attention to the risk of multifocal leukoencephalopathy development with stratification of risks.

тат (копаксон) по-прежнему остаются препаратами первого ряда. Копаксон – единственный препарат, который более 10 лет изучался в непрерывном про-долженном исследовании. Представлены результаты 20-летнего наблюдения 74 пациентов из пилотного американского исследования, изначально включаю-щего 232 больных. Продолжительность применения копаксона у них составила в среднем 27,3 года. Сред-негодовая частота обострений за время наблюдения была 0,2. Не имели обострений 24,3% пациентов. Средний балл по шкале eDSS за 20 лет увеличился с 2,4 только до 3,1. У 63% больных он остается ниже 4,0 баллов, у 79,5% – ниже 6 баллов. Подтвержден-ное прогрессирование отмечено у 47% пациентов (ford c. и соавт.). В закончившемся исследовании АDVANce с участием 1512 пациентов применяли пегилирован

The review presents the data on increasing the incidence of multiple sclerosis (MS) and possible causes of the increase. Possible modifying and non-modifying risk factors of MS are reviewed. The article presents the new data concerning value of grey matter lesions in brain and spinal cord, brain atrophy and biomarkers that could help in MS diagnosis and prediction of treatment response. Recently introduced terms “radiologically isolated syndrome” and “cortical relapses” are discussed. The difficulties in differential diagnosis between MS and similar diseases as neuromyelitis optica are presented. The differences between aquaporin-4 positive and negative patients with neuromyelitis optica are presented.

JC virus can exist in latent state in human bodies of many people. It can be activated in subjects with immunodeficiency and manifest with progressive multifocal leukoencephalopathy (PML) and some other neurological symptoms of central nervous system disorder. Most frequently people with AIDS suffer from JC virus. Reactivation of JC virus has recently been seen on immunosuppressive therapy. The article presents literature review of clinical and neuroimaging symptoms of PML associated with high-active HIV antiretrovirus therapy and natalizumab therapy of multiple sclerosis. The article also presents the inflammatory syndrome of immunity recovery.

Sarcoidosis is not often associated with damage of nervous system. The article presents a rare case report of sarcoidosis with spinal cord lesion in a young man. The disease manifested with rapid ascendant myelopathy. Intramedullar hyperintensive lesion with spinal block was revealed on T2-weighted tomogram. The patient has the symptoms of brain damage but brain lesions were not revealed on MRI scans. The diagnostic challenges are highlighted in the article. The differential diagnosis is conducted with transverse myelitis, multiple sclerosis, neuromyelitis optica, spinal cord tumor. The management algorithm of patients with sarcoidosis is reported. The efficacy of corticosteroids and cytostatic drugs is highlighted.

Clinical presentations, diagnosis and differential diagnosis of optic neuritis of different etiology are reviewed. This symptom is concomitant with the development of multiple sclerosis in about 30% cases and accompanies the disease in 75% patients. Acute or subacute lesion of the optic nerve can be a symptom of optic myelitis, Leber's disease, systemic lupus erythematosus, Susac's syndrome, idiopathic retinal vasculitis, sarcoidosis and some other diseases. Clinical features and course of optic neuritis in these diseases are discussed.

The two-phase model of the pathogenesis of multiple sclerosis (MS) is discussed in the aspect of inflammation and neurodegeneration processes. In the first phase, there are inflammation processes with frequent exacerbations and remissions and multiple lesions on MRI. An axonal lesion (neurodegeneration) is seen in this stage, even in the very beginning, i.e. in the stage of clinically isolated syndrome. The possibilities of treatment of neurodegenerative changes, in particular, with glatiramer acetate (GA) or copaxon, are reviewed. Copaxon induces a switch from Th1-cells to GA-specific Th2-lymphocyte production which can produce neurotrophic factors. Clinical and MRI data as well as experimental results supporting the neuroprotective effect of this drug are presented.